The long-term objective of this research is to provide a biochemical mechanism for cataract caused by an overdose of the essential trace mineral, selenium. Experiments will be performed to test our working hypothesis for the mechanism of selenite cataract. This hypothesis states that the association of selenium with critical lens proteins in the epithelium or lens bow region initiates a chain of events leading to accumulation of calcium in the nucleus and subsequent nuclear opacity. Four experiments will study: 1) the association of 75Se with lens proteins, 2) the effect of selenium on lens proteins, 3) the role of calcium in selenite cataractogenesis, and 4) the histological basis of selenite cataract. When possible, human lenses will be subjected to studies performed on rat lenses. Not only will these studies provide a biochemical basis for selenite cataract, but they will provide a study system for measuring the role of calcium in cataractogenesis, devoid of changes in lens sodium, potassium, and water. Hopefully, these model studies will help to understand and prevent cataractogenesis in man.